Rhod-2 (sodium salt)
目录号 : GC44828A red fluorescent calcium indicator
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >90.00%
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- Datasheet
Rhod-2 (sodium salt) is a water-soluble, red fluorescent calcium indicator. It exhibits a significant shift in fluorescence intensity upon calcium binding (ex max = 549 nm; calcium-free v. ex/em max = 552/581 nm; calcium-bound). [1][2] Unlike the UV-excitable indicators fura-2 and indo-1 , there is no accompanying spectral shift.
Reference:
[1]. Paredes, R.M., Etzler, J.C., Watts, L.T., et al. Chemical calcium indicators. Methods 46(3), 143-151 (2008).
[2]. Minta, A., Kao, J.P., and Tsien, R.Y. Fluorescent indicators for cytosolic calcium based on rhodamine and fluorescein chromophores. The Journal of Biological Chemisty 264(14), 8171-8178 (1989).
Cas No. | SDF | ||
化学名 | 2,2'-((2-(2-(2-(bis(carboxylatomethyl)amino)-5-(6-(dimethylamino)-3-(dimethyliminio)-3H-xanthen-9-yl)phenoxy)ethoxy)-4-methylphenyl)azanediyl)diacetate, trisodium salt | ||
Canonical SMILES | CN(C)C(C=C1)=CC2=C1C(C3=CC=C(N(CC([O-])=O)CC([O-])=O)C(OCCOC4=C(N(CC([O-])=O)CC([O-])=O)C=CC(C)=C4)=C3)=C(C=C/5)C(O2)=CC5=[N+](C)\C.[Na+].[Na+].[Na+] | ||
分子式 | C40H39N4O11•3Na | 分子量 | 820.7 |
溶解度 | moderately soluble in water | 储存条件 | Store at -20°C |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
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Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 |
制备储备液 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 1.2185 mL | 6.0924 mL | 12.1847 mL |
5 mM | 0.2437 mL | 1.2185 mL | 2.4369 mL |
10 mM | 0.1218 mL | 0.6092 mL | 1.2185 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
计算重置 |
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工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
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Mode of mitochondrial Ca2+ clearance and its influence on secretory responses in stimulated chromaffin cells
Cell Calcium 2006 Jan;39(1):35-46.PMID:16257445DOI:10.1016/j.ceca.2005.09.001.
To study the role of mitochondrial Ca(2+) clearance in stimulated cells, changes in free Ca(2+) concentration in the cytosol, [Ca(2+)](c) and that in mitochondria, [Ca(2+)](m) along with secretory responses were observed using chromaffin cells co-loaded with Fura-2 and Rhod-2 in the perfused rat adrenal medulla. When the cells were stimulated with 40 mM K(+) in the perfusate, the duration of [Ca(2+)](m) response markedly increased with prolongation of the stimulation period, exhibiting a mean half-decay time of 21 min with 30s stimulation, whereas its amplitude was not altered with stimulations of 10-30s. A computer simulation analysis showed that such a mode of [Ca(2+)](m) response can be produced if excess Ca(2+) taken up by mitochondria precipitates as calcium phosphate (Pi) salt. In the presence of 5 microM rotenone plus 10 microM oligomycin, a decrease in the duration of [Ca(2+)](m) response and a slight but significant increase (24%) in the secretory response to 30s stimulation with 40 mM K(+) were observed. Simulation analyses suggested that this effect of rotenone may be due to reduction in mitochondrial Ca(2+) uptake induced by rotenone-elicited partial depolarization of the mitochondrial membrane potential. In chromaffin cells transsynaptically stimulated through the splanchnic nerve, the intensity of NAD(P)H autofluorescence changed with time courses similar to those of [Ca(2+)](m) responses. The temporal profiles of those two responses were prolonged in a similar manner by application of an inhibitor of mitochondrial Na(+)/Ca(2+) exchanger, CGP37157. Thus, due to the unique Ca(2+) buffering mechanism, [Ca(2+)](m) responses associated with massive mitochondrial Ca(2+) uptake may occur within a limited concentration range in which Ca(2+)-sensitive dehydrogenases are activated to control the mitochondrial redox state in stimulated chromaffin cells.
Mitochondrial Ca2+ uptake and release influence metabotropic and ionotropic cytosolic Ca2+ responses in rat oligodendrocyte progenitors
J Physiol 1998 Apr 15;508 ( Pt 2)(Pt 2):413-26.PMID:9508806DOI:10.1111/j.1469-7793.1998.413bq.x.
1. Many physiologically important activities of oligodendrocyte progenitor cells (O-2A cells), including proliferation, migration and differentiation, are regulated by cytosolic Ca2+ signals. However, little is known concerning the mechanisms of Ca2+ signalling in this cell type. We have studied the interactions between Ca2+ entry, Ca2+ release from endoplasmic reticulum and Ca2+ regulation by mitochondria in influencing cytosolic Ca2+ responses in O-2A cells. 2. Methacholine (MCh; 100 microM) activated Ca2+ waves that propagated from several initiation sites along O-2A processes. 3. During a Ca2+ wave evoked by MCh, mitochondrial membrane potential was often either depolarized (21 % of mitochondria) or hyperpolarized (20 % of mitochondria), as measured by changes in the fluorescence of 5,5',6,6'-tetrachloro-1,1',3, 3'-tetraethylbenzimidazole carbocyanine iodide (JC-1). 4. Stimulation with kainate (100 microM) evoked a slowly rising, sustained cytosolic Ca2+ elevation in O-2A cells. This also, in some cases, resulted in either a depolarization (15 % of mitochondria) or hyperpolarization (12 % of mitochondria) of mitochondrial membrane potential. 5. Simultaneous measurement of cytosolic (fluo-3 AM) and mitochondrial (Rhod-2 AM) Ca2+ responses revealed that Ca2+ elevations in the cytosol evoked by either MCh or kainate were translated into long-lasting Ca2+ elevations in subpopulations of mitochondria. In some mitochondria, Ca2+ signals appeared to activate Ca2+ release into the cytosol. 6. Inhibition of the mitochondrial Na+-Ca2+ exchanger by CGP-37157 (25 microM) decreased kainate Ca2+ response amplitude and increased the rate of return of the response to basal Ca2+ levels. 7. Thus, both ionotropic and metabotropic stimulation evoke changes in mitochondrial membrane potential and Ca2+ levels in O-2A cells. Ca2+ uptake into some mitochondria is activated by Ca2+ entry into cells or release from stores. Mitochondrial Ca2+ release appears to play a key role in shaping kainate-evoked Ca2+ responses.